Abstract:We investigated the effects of low-dose granulocyte colony-stimulating factor (G-CSF) on the mobilization of stem cells in 6 healthy subjects. When G-CSF was administered by continuous subcutaneous infusion at a rate of 72 microg/day for 5 days, the numbers of white blood cells and granulocytes rapidly increased to maximal levels. CD34+ cells were mobilized to the peripheral blood in 3 days, and the maximal level was reached 4 or 5 days after the start of treatment. We attempted to determine whether the levels… Show more
“…It has been reported that G-CSF induces the mobilization of BMSCs from BM into the peripheral blood circulation (17). There were more capillaries in the border area of all the cytokine treatment groups with G-CSF than in control group after MI, and a part of the cells constituting the capillary wall were derived from BM cells.…”
Pretreatment with a combination of granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) has been reported to attenuate left ventricular (LV) remodeling after acute myocardial infarction (MI). We here examined whether the cytokine treatment started after MI has also beneficial effects. Anterior MI was created in the recipient mice whose bone marrow had been replaced with that of transgenic mice expressing enhanced green fluorescent protein (GFP). We categorized mice into five groups according to the following treatment: 1) saline; 2) administration of G-CSF and SCF from 5 days before MI through 3 days after; 3) administration of G-CSF and SCF for 5 days after MI; 4) administration of G-CSF alone for 5 days after MI; 5) administration of SCF alone for 5 days after MI. All the three treatment groups with G-CSF showed less LV remodeling and improved cardiac function and survival rate after MI. The number of capillaries, which express GFP, was increased and the number of apoptotic cells was decreased in the border area of all the treatment groups with G-CSF. Even if the cytokine treatment is started after MI, it could prevent LV remodeling and dysfunction after MI--at least in part--through an increase in neovascularization and a decrease in apoptosis in the border area.
“…It has been reported that G-CSF induces the mobilization of BMSCs from BM into the peripheral blood circulation (17). There were more capillaries in the border area of all the cytokine treatment groups with G-CSF than in control group after MI, and a part of the cells constituting the capillary wall were derived from BM cells.…”
Pretreatment with a combination of granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) has been reported to attenuate left ventricular (LV) remodeling after acute myocardial infarction (MI). We here examined whether the cytokine treatment started after MI has also beneficial effects. Anterior MI was created in the recipient mice whose bone marrow had been replaced with that of transgenic mice expressing enhanced green fluorescent protein (GFP). We categorized mice into five groups according to the following treatment: 1) saline; 2) administration of G-CSF and SCF from 5 days before MI through 3 days after; 3) administration of G-CSF and SCF for 5 days after MI; 4) administration of G-CSF alone for 5 days after MI; 5) administration of SCF alone for 5 days after MI. All the three treatment groups with G-CSF showed less LV remodeling and improved cardiac function and survival rate after MI. The number of capillaries, which express GFP, was increased and the number of apoptotic cells was decreased in the border area of all the treatment groups with G-CSF. Even if the cytokine treatment is started after MI, it could prevent LV remodeling and dysfunction after MI--at least in part--through an increase in neovascularization and a decrease in apoptosis in the border area.
“…Cytokines and growth factors other than GM-CSF populate the tumor microenvironment and diffuse systemically in tumor-bearing hosts. CSF such as G-CSF, a glycoprotein that stimulates the release of white blood cells, particularly granulocytes and hematopoietic stem cells, into peripheral blood (54,55), is produced by squamous cells carcinomas of esophagus and tongue (56) and head and neck carcinomas (57,58). M-CSF, also known as CSF-1, has been detected in several human neoplasias such as acute myeloblastic leukemia (59,60), renal cell carcinoma (61), bladder carcinoma (62), and breast cancer, in which it seems to favor tumor progression and correlate with poor prognosis (63).…”
Section: Mdsc Recruiting and Activating Factorsmentioning
Emerging evidence indicates that the Achilles' heel of cancer immunotherapies is often the complex interplay of tumor-derived factors and deviant host properties, which involve a wide range of immune elements in the lymphoid and myeloid compartments. Regulatory lymphocytes, tumor-conditioned myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages, and dysfunctional and immature dendritic cells take part in a complex immunoregulatory network. Despite the fact that some mechanisms governing tumor-induced immune tolerance and suppression are starting to be better understood and their complexity dissected, little is known about the diachronic picture of immune tolerance. Based on observations of MDSCs, we present a time-structured and topologically consistent idea of tumor-dependent tolerance progression in tumor-bearing hosts.
“…Bone marrow stem cells (BMSCs) differentiate into cardiomyocytes and endothelial cells and may participate in the regeneration of cardiac lesions (1)(2)(3)(4). Granulocyte colonystimulating factor (G-CSF) increased the number of peripheral granulocytes (5) and induced the mobilization of BMSCs to the periphery (6). This property and regenerative capacity of BMSCs justify the efforts to prove the efficacy of this therapy.…”
This study investigates the effects of granulocyte colony-stimulating factor (G-CSF) therapy in experimental chronic chagasic cardiomyopathy. Chagas disease is one of the leading causes of heart failure in Latin America and remains without an effective treatment other than cardiac transplantation. C57BL/6 mice were infected with 10(3) trypomastigotes of Trypanosoma cruzi, and chronic chagasic mice were treated with G-CSF or saline (control). Evaluations following treatment were functional, immunological, and histopathological. Comparing hearts of G-CSF-treated mice showed reduced inflammation and fibrosis compared to saline-treated chagasic mice. G-CSF treatment did not alter the parasite load but caused an increase in the number of apoptotic inflammatory cells in the heart. Cardiac conductance disturbances in all infected animals improved or remained stable due to the G-CSF treatment, whereas all of the saline-treated mice deteriorated. The distance run on a treadmill and the exercise time were significantly greater in G-CSF-treated mice when compared to chagasic controls, as well as oxygen consumption (VO(2)), carbon dioxide production (VCO(2)), and respiratory exchange ration (RER) during exercise. Administration of G-CSF in experimental cardiac ischemia had beneficial effects on cardiac structure, which were well correlated with improvements in cardiac function and whole animal performance.
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